Fed male Sprague Dawley rats were given 7.5 gm. ethanol/kg body weight or an isocaloric amount of glucose. Serum triglycerides reached their peak of 2 1/2 fold elevation by 2 hours and fell to normal levels at 4 hours. Liver slices prepared 2 hours after the ethanol or glucose showed no difference in the rate of fatty acid synthesis from acetate-1-C14 or palmitate-1-C14 oxidation. The rate of synthesis of lipoproteins in d less than 1.006, d equals 1.006-1.063 and d greater than 1.063 in vivo from either a C14-amino acid hydrolysate or C14-palmitate was the same in the ethanol and glucose treated animal 2 hours later. Post-heparin lipolytic activity and fatty acid release from adipose tissue was not altered by the ethanol. Significantly more ethanol than glucose per os was incorporated in hepatic and serum lipid 2 hours later. In liver slices the rate of lipid synthesis from ethanol was over 3 times greater than from glucose over 3 hours. Liver microsomes prepared from rats 1 or 2 hours after ethanol incorporated significantly more C14-palmitate into triglycerides than microsomes from glucose treated animals. Thus alcohol-induced hypertriglyceridemia in rats appears due to the liver synthesizing more fatty acids from ethanol than from glucose and liver microsomes synthesizing more triglycerides as a result of ethanol administration. BIBLIOGRAPHIC REFERENCES: Gryboski, Joyce D, Scheig, Robert, Schwartz, Allen and Spackman, Thomas J. Gastrointestinal Problems in the Infant. W.B. Saunders Co., Philadelphia Pa, 1975. pp 311-449. Scheig, Robert. Changes in Sexual Performance due to Liver Disease. Medical Aspects of Human Sexuality, pp 67-79, April 1975.